The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
The paradox of autophagy and its implication in cancer etiology and therapy
Open accessAbstract
Autophagy is a cellular self-catabolic process in which cytoplasmic constituents are sequestered in double membrane vesicles that fuse with lysosomes where they are degraded. As this catabolic activity generates energy, autophagy is often induced under nutrient limiting conditions providing a mechanism to maintain cell viability and may be exploited by cancer cells for survival under metabolic stress. However, progressive autophagy can be cytotoxic and autophagy can under certain settings substitute for apoptosis in induction of cell death. Moreover, loss of autophagy is correlated with tumorigenesis and several inducers of autophagy are tumor-suppressor genes. Thus, the relation of autophagy to cancer development is complex and depends on the genetic composition of the cell as well as on the extra-cellular stresses a cell is exposed to. In this review we describe the intricate nature of autophagy and its regulators, particularly those that have been linked to cancer. We discuss the multifaceted relation of autophagy to tumorigenesis and highlight studies supporting a role for autophagy in both tumor-suppression and tumor-progression. Finally, various autophagy-targeting therapeutic strategies for cancer treatment are presented.
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Cites
Suppression of basal autophagy in neural cells causes neurodegenerative disease in mice
Hara, T., Nakamura, K., Matsui, M., Yamamoto, A., Nakahara, Y., Suzuki-Migishima, R., Yokoyama, M., Mishima, K., Saito, I., Okano, H., et al. (2006) · Nature · doi:10.1038/nature04724 · Cited by 3,882
Loss of autophagy in the central nervous system causes neurodegeneration in mice
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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
Inoki, K., Li, Y., Zhu, T., Wu, J., & Guan, K.-L. (2002) · Nature Cell Biology · doi:10.1038/ncb839 · Cited by 3,083
The role of autophagy during the early neonatal starvation period
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Promotion of tumorigenesis by heterozygous disruption of the beclin 1 autophagy gene
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Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4
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“Examples of these include etoposide, an inducer of p53-dependent apoptosis, that was shown to induce autophagy in mouse embryonic fibroblasts in a p53-dependent manner [89]; Ligation of the TRAIL receptor-2 by human scFv antibody triggered autophagic cell death in both TRAIL-sensitive and TRAILresistant cancer cells […”
BackgroundRheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling
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Cited by
Reactive Oxygen Species-Induced Lipid Peroxidation in Apoptosis, Autophagy, and Ferroptosis
Su, L.-J., Zhang, J.-H., Gomez, H., Murugan, R., Hong, X., Xu, D., Jiang, F., & Peng, Z.-Y. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/5080843 · Cited by 2,166
Regulation of autophagy by ROS: physiology and pathology
Scherz-Shouval, R., & Elazar, Z. (2011) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2010.07.007 · Cited by 1,263
Cell death-based treatment of lung adenocarcinoma
Denisenko, T. V., Budkevich, I. N., & Zhivotovsky, B. (2018) · Cell Death & Disease · doi:10.1038/s41419-017-0063-y · Cited by 768
Dual role of autophagy in hallmarks of cancer
Singh, S. S., Vats, S., Chia, A. Y.-Q., Tan, T. Z., Deng, S., Ong, M. S., Arfuso, F., Yap, C. T., Goh, B. C., Sethi, G., et al. (2018) · Oncogene · doi:10.1038/s41388-017-0046-6 · Cited by 542
Berberine: New perspectives for old remedies
Tillhon, M., Guamán Ortiz, L. M., Lombardi, P., & Scovassi, A. I. (2012) · Biochemical Pharmacology · doi:10.1016/j.bcp.2012.07.018 · Cited by 477
Metadata
- Authors
- Eisenberg-Lerner, A., & Kimchi, A.
- Venue
- Apoptosis
- Published
- 2009-01-27
- Volume
- 14
- Issue
- 4
- Pages
- 376-391
- ISSN
- 1360-8185 (ISSN-L)
- 1573-675X
- OpenAlex
- W1966238464
- Cited by
- 213
- References
- 29
- FWCI
- 15.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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